Hyperplastic polyp | |
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Micrograph of hyperplastic polyp | |
Specialty | Gastroenterology |
Symptoms | Usually asymptomatic |
Complications | Colorectal cancer |
Types | Microvesicular type [1] Goblet cell–rich type [1] |
Diagnostic method | Colonoscopy |
Differential diagnosis | Colorectal adenoma, Traditional serrated adenoma |
A hyperplastic polyp is a type of gastric polyp or colorectal polyp.
Most hyperplastic polyps are found in the distal colon and rectum. [2] They have no malignant potential, [2] which means that they are no more likely than normal tissue to eventually become a cancer.[ citation needed ]
Hyperplastic polyps on the right side of the colon do exhibit a malignant potential. This occurs through multiple mutations that affect the DNA-mismatch-repair pathways. As such DNA mutations during replication are not repaired. This leads to microsatellite instability which can eventually lead to malignant transformation in polyps on the right side of the colon.[ citation needed ]
Serrated polyposis syndrome is a rare condition that has been defined by the World Health Organization as either: [3]
Histopathologically, there are two main types of hyperplastic polyps, which have genetic differences, as well as different histologic structure, but no significant differences clinically. [4] The two main types of hyperplastic polyps are microvesicular mucin-rich type and goblet cell-rich type. [1] A mucin-poor type with eosinophilic cytoplasm, which is rare, was previously described. [4] However, the mucin poor type is no longer considered a distinct subtype. [1]
The luminal portion has a serrated ("saw tooth") appearance formed by tufts or folds of abundant apical cytoplasm. It contains glands with star-shaped lumina. [4] There are crypts that are elongated but straight, narrow and hyperchromatic at the base. All crypts reach to the muscularis mucosae. [4] The basement membrane is frequently thickened. [4]
Elongated, fat crypts and little to no serration. Therefore, they may not be obvious without comparing to adjacent normal intestinal wall. [4]
They are filled with goblet cells, extending to surface, which commonly has a tufted appearance. [4]
Infrequently, the epithelium is misplaced into the submucosa. Such polyps are termed "inverted hyperplastic polyps". They appear to be restricted to the sigmoid colon and rectum. The misplaced epithelium is mucin-depleted, similar to the basal one-third of the polyp. The misplacement is accompanied by the lamina propria and is continuous with the overlying polyp through a gap in the muscularis mucosae. It may require slices at multiple levels to demonstrate microscopically. [4]
In such cases adjacent bleeding and hemosiderin deposition is common. Collagen type IV stain will have a strong continuous staining around nests. [4]
Nuclei are small, regular, round and basal in the luminal half of the crypts, most reliably evaluated near the luminal surface. [4]
There are proliferative changes at the base of crypts, where nuclei are enlarged, the nucleus/cytoplasm ratio is elevated. [4]
Immunohistochemistry using Ki-67 stains the basal 1⁄3 to 1⁄2 of crypts, indicating a proliferative zone. [4]
The deep proliferative zones and reactive processes closely mimic changes seen in colorectal adenomas. [4]
Features that distinguish a hyperplastic polyp from a tubular colorectal adenoma are as follows:
Hyperplastic Polyp [4] | Tubular Adenoma [4] |
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Nu dysplasia | Dysplasia |
Proliferative epithelium restricted to base | Proliferative epithelium present at the surface |
Gland lining cells mature at the surface | No surface maturation |
A sessile serrated adenoma or traditional serrated adenoma is suspected if there is either of the following: [4]
A sessile serrated adenoma is suspected in case of any of the following: [4]
If both are present, it is almost always an SSA. Other features causing a suspicion for sessile serrated adenoma are: [4]
A polyp is an abnormal growth of tissue projecting from a mucous membrane. If it is attached to the surface by a narrow elongated stalk, it is said to be pedunculated; if it is attached without a stalk, it is said to be sessile. Polyps are commonly found in the colon, stomach, nose, ear, sinus(es), urinary bladder, and uterus. They may also occur elsewhere in the body where there are mucous membranes, including the cervix, vocal folds, and small intestine. Some polyps are tumors (neoplasms) and others are non-neoplastic, for example hyperplastic or dysplastic, which are benign. The neoplastic ones are usually benign, although some can be pre-malignant, or concurrent with a malignancy.
An adenoma is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both. Adenomas can grow from many glandular organs, including the adrenal glands, pituitary gland, thyroid, prostate, and others. Some adenomas grow from epithelial tissue in nonglandular areas but express glandular tissue structure. Although adenomas are benign, they should be treated as pre-cancerous. Over time adenomas may transform to become malignant, at which point they are called adenocarcinomas. Most adenomas do not transform. However, even though benign, they have the potential to cause serious health complications by compressing other structures and by producing large amounts of hormones in an unregulated, non-feedback-dependent manner. Some adenomas are too small to be seen macroscopically but can still cause clinical symptoms.
Gardner's syndrome is a subtype of familial adenomatous polyposis (FAP). Gardner syndrome is an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon. The extracolonic tumors may include osteomas of the skull, thyroid cancer, epidermoid cysts, fibromas, as well as the occurrence of desmoid tumors in approximately 15% of affected individuals.
Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated. Three variants are known to exist, FAP and attenuated FAP are caused by APC gene defects on chromosome 5 while autosomal recessive FAP is caused by defects in the MUTYH gene on chromosome 1. Of the three, FAP itself is the most severe and most common; although for all three, the resulting colonic polyps and cancers are initially confined to the colon wall. Detection and removal before metastasis outside the colon can greatly reduce and in many cases eliminate the spread of cancer.
A benign tumor is a mass of cells (tumor) that does not invade neighboring tissue or metastasize. Compared to malignant (cancerous) tumors, benign tumors generally have a slower growth rate. Benign tumors have relatively well differentiated cells. They are often surrounded by an outer surface or stay contained within the epithelium. Common examples of benign tumors include moles and uterine fibroids.
A precancerous condition is a condition, tumor or lesion involving abnormal cells which are associated with an increased risk of developing into cancer. Clinically, precancerous conditions encompass a variety of abnormal tissues with an increased risk of developing into cancer. Some of the most common precancerous conditions include certain colon polyps, which can progress into colon cancer, monoclonal gammopathy of undetermined significance, which can progress into multiple myeloma or myelodysplastic syndrome. and cervical dysplasia, which can progress into cervical cancer. Bronchial premalignant lesions can progress to squamous cell carcinoma of the lung.
Fundic gland polyposis is a medical syndrome where the fundus and the body of the stomach develop many fundic gland polyps. The condition has been described both in patients with familial adenomatous polyposis (FAP) and attenuated variants (AFAP), and in patients in whom it occurs sporadically.
Juvenile polyposis syndrome is an autosomal dominant genetic condition characterized by the appearance of multiple juvenile polyps in the gastrointestinal tract. Polyps are abnormal growths arising from a mucous membrane. These usually begin appearing before age 20, but the term juvenile refers to the type of polyp, not to the age of the affected person. While the majority of the polyps found in juvenile polyposis syndrome are non-neoplastic, hamartomatous, self-limiting and benign, there is an increased risk of adenocarcinoma.
A colorectal polyp is a polyp occurring on the lining of the colon or rectum. Untreated colorectal polyps can develop into colorectal cancer.
A sessile serrated lesion (SSL) is a premalignant flat lesion of the colon, predominantly seen in the cecum and ascending colon.
Colon cancer staging is an estimate of the amount of penetration of a particular cancer. It is performed for diagnostic and research purposes, and to determine the best method of treatment. The systems for staging colorectal cancers depend on the extent of local invasion, the degree of lymph node involvement and whether there is distant metastasis.
Rectal discharge is intermittent or continuous expression of liquid from the anus. Normal rectal mucus is needed for proper excretion of waste. Otherwise, this is closely related to types of fecal incontinence but the term rectal discharge does not necessarily imply degrees of incontinence. Types of fecal incontinence that produce a liquid leakage could be thought of as a type of rectal discharge.
The colorectal adenoma is a benign glandular tumor of the colon and the rectum. It is a precursor lesion of the colorectal adenocarcinoma. They often manifest as colorectal polyps.
McKittrick-Wheelock syndrome is an uncommon syndrome caused by large, villous adenomas that secrete high quantities of electrolyte-rich mucin. This may lead to pre-renal acute kidney injury, secretory diarrhea, and dehydration. It is estimated that 2-3% of large villous adenomas, typically greater than 4 cm in diameter, will present with this hypersecretory pattern.
MUTYH-associated polyposis is an autosomal recessive polyposis syndrome. The disorder is caused by mutations in both alleles of the DNA repair gene, MUTYH. The MUTYH gene encodes a base excision repair protein, which corrects oxidative damage to DNA. Affected individuals have an increased risk of colorectal cancer, precancerous colon polyps (adenomas) and an increased risk of several additional cancers. About 1–2 percent of the population possess a mutated copy of the MUTYH gene, and less than 1 percent of people have the MUTYH-associated polyposis syndrome. The presence of 10 or more colon adenomas should prompt consideration of MUTYH-associated polyposis, familial adenomatous polyposis and similar syndromes.
The histopathology of colorectal cancer of the adenocarcinoma type involves analysis of tissue taken from a biopsy or surgery. A pathology report contains a description of the microscopical characteristics of the tumor tissue, including both tumor cells and how the tumor invades into healthy tissues and finally if the tumor appears to be completely removed. The most common form of colon cancer is adenocarcinoma, constituting between 95% and 98% of all cases of colorectal cancer. Other, rarer types include lymphoma, adenosquamous and squamous cell carcinoma. Some subtypes have been found to be more aggressive.
Serrated polyposis syndrome (SPS), previously known as hyperplastic polyposis syndrome, is a disorder characterized by the appearance of serrated polyps in the colon. While serrated polyposis syndrome does not cause symptoms, the condition is associated with a higher risk of colorectal cancer (CRC). The lifelong risk of CRC is between 25 and 40%. SPS is the most common polyposis syndrome affecting the colon, but is under recognized due to a lack of systemic long term monitoring. Diagnosis requires colonoscopy, and is defined by the presence of either of two criteria: five or more serrated lesions/polyps proximal to the rectum, or more than 20 serrated lesions/polyps of any size distributed throughout the colon with five proximal to the rectum.
Polymerase proofreading-associated polyposis (PPAP) is an autosomal dominant hereditary cancer syndrome, which is characterized by numerous polyps in the colon and an increased risk of colorectal cancer. It is caused by germline mutations in DNA polymerase ε (POLE) and δ (POLD1). Affected individuals develop numerous polyps called colorectal adenomas. Compared with other polyposis syndromes, Polymerase proofreading-associated polyposis is rare. Genetic testing can help exclude similar syndromes, such as Familial adenomatous polyposis and MUTYH-associated polyposis. Endometrial cancer, duodenal polyps and duodenal cancer may also occur.
Traditional serrated adenoma is a premalignant type of polyp found in the colon, often in the distal colon. Traditional serrated adenomas are a type of serrated polyp, and may occur sporadically or as a part of serrated polyposis syndrome. Traditional serrated adenomas are relatively rare, accounting for less than 1% of all colon polyps. Usually, traditional serrated adenomas are found in the distal colon and are usually less than 10 mm in size.
Juvenile polyps are a type of polyp found in the colon. While juvenile polyps are typically found in children, they may be found in people of any age. Juvenile polyps are a type of hamartomatous polyps, which consist of a disorganized mass of tissue. They occur in about two percent of children. Juvenile polyps often do not cause symptoms (asymptomatic); when present, symptoms usually include gastrointestinal bleeding and prolapse through the rectum. Removal of the polyp (polypectomy) is warranted when symptoms are present, for treatment and definite histopathological diagnosis. In the absence of symptoms, removal is not necessary. Recurrence of polyps following removal is relatively common. Juvenile polyps are usually sporadic, occurring in isolation, although they may occur as a part of juvenile polyposis syndrome. Sporadic juvenile polyps may occur in any part of the colon, but are usually found in the distal colon. In contrast to other types of colon polyps, juvenile polyps are not premalignant and are not usually associated with a higher risk of cancer; however, individuals with juvenile polyposis syndrome are at increased risk of gastric and colorectal cancer. Unlike juvenile polyposis syndrome, solitary juvenile polyps do not require follow up with surveillance colonoscopy.